卵巢颗粒细胞中的丝裂原活化蛋白激酶3/1（细胞外信号调节激酶1/2）对雌性生育能力至关重要。
MAPK3/1 (ERK1/2) in ovarian granulosa cells are essential for female fertility.
作者信息
Fan Heng-Yu, Liu Zhilin, Shimada Masayuki, Sterneck Esta, Johnson Peter F, Hedrick Stephen M, Richards Joanne S
机构信息
Department of Molecular and Cellular Biology, Baylor College of Medicine, 1 Baylor Plaza, Houston, TX 77030, USA.
出版信息
Science. 2009 May 15;324(5929):938-41. doi: 10.1126/science.1171396.
Abstract
A surge of luteinizing hormone (LH) from the pituitary gland triggers ovulation, oocyte maturation, and luteinization for successful reproduction in mammals. Because the signaling molecules RAS and ERK1/2 (extracellular signal-regulated kinases 1 and 2) are activated by an LH surge in granulosa cells of preovulatory follicles, we disrupted Erk1/2 in mouse granulosa cells and provide in vivo evidence that these kinases are necessary for LH-induced oocyte resumption of meiosis, ovulation, and luteinization. In addition, biochemical analyses and selected disruption of the Cebpb gene in granulosa cells demonstrate that C/EBPbeta (CCAAT/Enhancer-binding protein-beta) is a critical downstream mediator of ERK1/2 activation. Thus, ERK1/2 and C/EBPbeta constitute an in vivo LH-regulated signaling pathway that controls ovulation- and luteinization-related events.
摘要
来自脑垂体的促黄体生成素（LH）激增会触发排卵、卵母细胞成熟和黄体化，从而使哺乳动物成功繁殖。由于信号分子RAS和ERK1/2（细胞外信号调节激酶1和2）在前排卵卵泡的颗粒细胞中被LH激增激活，我们在小鼠颗粒细胞中破坏了Erk1/2，并提供了体内证据，证明这些激酶对于LH诱导的卵母细胞减数分裂恢复、排卵和黄体化是必需的。此外，生化分析以及在颗粒细胞中对Cebpb基因的选择性破坏表明，C/EBPβ（CCAAT/增强子结合蛋白β）是ERK1/2激活的关键下游介质。因此，ERK1/2和C/EBPβ构成了一条体内LH调节的信号通路，该通路控制与排卵和黄体化相关的事件。
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